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R E S E A R C H Open AccessParental and household smoking and the increased risk of bronchitis, bronchiolitis and other lower respiratory infections in infancy: systematic review and met

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R E S E A R C H Open Access

Parental and household smoking and the

increased risk of bronchitis, bronchiolitis and

other lower respiratory infections in infancy:

systematic review and meta-analysis

Abstract

Background: Passive smoke exposure increases the risk of lower respiratory infection (LRI) in infants, but the extensive literature on this association has not been systematically reviewed for nearly ten years The aim of this paper is to provide an updated systematic review and meta-analysis of studies of the association between passive smoking and LRI, and with diagnostic subcategories including bronchiolitis, in infants aged two years and under Methods: We searched MEDLINE and EMBASE (to November 2010), reference lists from publications and abstracts from major conference proceedings to identify all relevant publications Random effect pooled odds ratios (OR) with 95% confidence intervals (CI) were estimated

Results: We identified 60 studies suitable for inclusion in the meta-analysis Smoking by either parent or other household members significantly increased the risk of LRI; odds ratios (OR) were 1.22 (95% CI 1.10 to 1.35) for paternal smoking, 1.62 (95% CI 1.38 to 1.89) if both parents smoked, and 1.54 (95% CI 1.40 to 1.69) for any

household member smoking Pre-natal maternal smoking (OR 1.24, 95% CI 1.11 to 1.38) had a weaker effect than post-natal smoking (OR 1.58, 95% CI 1.45 to 1.73) The strongest effect was on bronchiolitis, where the risk of any household smoking was increased by an OR of 2.51 (95% CI 1.96 to 3.21)

Conclusions: Passive smoking in the family home is a major influence on the risk of LRI in infants, and especially

on bronchiolitis Risk is particularly strong in relation to post-natal maternal smoking Strategies to prevent passive smoke exposure in young children are an urgent public and child health priority

Background

The 2006 US Surgeon General’s report on the effects of

involuntary exposure to tobacco smoke concluded that

passive smoking was a cause of a range of diseases of

children, including acute lower respiratory infection

(LRI) [1] Those conclusions were based in part on the

results of a series of systematic reviews and

meta-analyses first commissioned for a report by the UK

Gov-ernment Scientific Committee on Tobacco and Health

(SCOTH) [2], which were then updated for the Surgeon

General report The original meta-analysis of effects on

LRI was published by Strachan and Cook in 1997 [3] and included papers published to 1996; the update for the Surgeon General, as well as an updated SCOTH report published in 2004 [4], included papers published

to 2001

Since 2001, many more studies of this association have been published but have not as yet been subject to meta-analysis We have therefore updated the original Strachan and Cook review and meta-analyses of the epi-demiological data to provide contemporary estimates of the effect of passive smoking on LRI in infants in the first two years of life, and to use the larger evidence base to explore the effects of pre-natal and post-natal exposure, effects of smoking by either parent, both par-ents or by any household member, and the effects of

* Correspondence: laura.jones@nottingham.ac.uk

1 UK Centre for Tobacco Control Studies, Division of Epidemiology and Public

Health, University of Nottingham, Clinical Sciences Building, Nottingham City

Hospital, Nottingham, NG5 1PB, UK

Full list of author information is available at the end of the article

© 2011 Jones et al; licensee BioMed Central Ltd This is an Open Access article distributed under the terms of the Creative Commons Attribution License (http://creativecommons.org/licenses/by/2.0), which permits unrestricted use, distribution, and reproduction in

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passive smoking on subcategories of the LRI diagnostic

group The work was carried out as part of a more

extensive review of the effects of passive smoking in

children, for the Royal College of Physicians [5]

Methods

Systematic review methods

The search strategy employed in the original Strachan

and Cook systematic review and meta-analysis [3] was

repeated in the current study and included a

compre-hensive literature search of MEDLINE (1997 to

November 2010) and EMBASE (1997 to November

2010), published reviews, reference lists from identified

publications and abstracts from major conference

pro-ceedings (European Respiratory Society and American

Thoracic Society) No restrictions on language were

imposed during the searches, but in keeping with the

original strategy we report only results from papers

writ-ten and published in English [3] Studies of passive

smoking were selected by the MeSH heading tobacco

smoke pollution and/or relevant text words in the title,

keywords or abstract We then combined the results

from the searches with the studies identified and

included in the previous review [3]

Inclusion and exclusion criteria

Two authors (AH & TM, or AH & JLB) independently

reviewed the titles and abstracts identified from the

searches, and identified all studies meeting the following

inclusion criteria: (a) the design was a comparative

epi-demiological study (case-control, cross-sectional or

cohort design); (b) LRI, pneumonia, bronchitis,

bronch-iolitis or acute respiratory infection, either by parental

report or clinical diagnosis, was presented as an

out-come; (c) passive smoke exposure was ascertained by

self report and/or biochemical validation of parental

smoking We excluded studies that were not primary

reports (such as systematic reviews and commentaries);

or in which asthma, wheeze, proven infection with

respiratory syncytial virus rather than clinically

diag-nosed bronchiolitis, or death from LRI were identified

as the sole outcome; or in which the majority of infants

in the study were over the age of two years Following

the title and abstract review, two of three researchers

(LLJ, AH, and/or JLB) independently reviewed the full

text, excluding irrelevant papers as appropriate

Dis-agreements were resolved through group discussion

Data relating to study design, methods, definition of LRI

outcome, characteristics of reference group,

ascertain-ment of passive smoke exposure, passive smoke source,

and timing of exposure, location of study, and age of

study population, were extracted using a previously

piloted data extraction form and entered into a

standar-dised database

Assessment of methodological quality Studies that met the inclusion criteria were indepen-dently scored for methodological quality using the Cochrane Collaboration Non-Randomized Studies Working Group recognised Newcastle-Ottawa Quality Assessment Scale [6] by two reviewers This scale is based on three broad categories relating to the selection

of the study sample (four points); the comparability of the sample groups (two points); and the ascertainment

of either the exposure (for case-control (three points) and cross-sectional studies (two points)) or the outcome (for cohort studies (three points) Thus, cross-sectional studies were rated out of a total of eight points and case-control and cohort studies out of a total of nine points A score of seven or more was chosena priori to indicate high methodological quality

Statistical analysis Data were analyzed to yield effect estimates either using unadjusted (crude) odds ratios (OR) from extracted data from the publications, or where possible, adjusted ORs Meta-analysis was carried out to estimate the effects on the risk of LRI of smoking by the mother only, father only, both parents, and any household member Studies which clearly defined maternal smoking as pre- or post-natal were analysed separately Random effects models [7] were used to calculate a pooled OR with 95% confi-dence intervals (CI) because the effect estimates were expected to be heterogeneous due to differences in the populations and exposures in the studies Heterogeneity between study estimates was assessed using established methods (I2) [8] To explore reasons for heterogeneity between the studies, sub-group analyses were used to assess the roles of disease outcome (LRI, pneumonia, bronchitis, bronchiolitis, or acute respiratory infection), study type (cohort, cross-sectional, or case-control), study publication date (pre versus post 1997), methodo-logical quality (lower versus higher), and method of ascertainment of passive smoke exposure (self reported versus biochemical validation) Publication bias was assessed visually using a funnel plot for the association between exposure to household passive smoke and the risk of LRI Data were analyzed using Review Manager, version 5.0.23 ((RevMan), Copenhagen, The Nordic Cochrane Centre, The Cochrane Collaboration)

P values less than 0.05 were considered statistically sig-nificant This analysis was performed in accordance with the Meta-Analysis of Observational Studies in Epide-miology (MOOSE) guidelines [9]

Results Our post 1997 literature searches identified an initial sample of 3236 papers, of which 132 were deemed eli-gible for further review on the basis of their title and

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abstract One hundred and three of these studies were

excluded after full text review because they were

either: [a] not primary studies but editorials, letters or

commentaries; [b] the majority of infants in the study

sample were older than two years; [c] the definition of

the outcome was not lower respiratory infection; or [d]

there were insufficient or unusable data presented in

the paper We thus identified a total of 29 papers

pub-lished between 1997 and the end of November 2010

which met our inclusion criteria of a comparative

epidemiological study assessing passive smoke expo-sure and the risk of lower respiratory infection in infants less than two years of age Of the 38 papers included in the original Strachan and Cook meta-ana-lysis [3], seven did not meet our inclusion criteria, because wheeze was recorded as the primary outcome [10-15], or there were problems with recall bias [16]

We thus identified a total of 60 studies for inclusion in the present meta-analysis [see Additional file 1 and Figure 1]

31 studies included from

Strachan and Cook Review

3236 studies retrieved from initial Medline and Embase database search

2604 excluded after title review

632 abstracts reviewed

500 excluded after abstract review

132 full texts reviewed

103 excluded after full text review

29 studies included in

updated meta-analysis

60 studies included in updated meta-analysis

Figure 1 Flow diagram of included and excluded studies.

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Over half of the included studies [17-47] used data from

cohorts, primarily birth cohorts; 15 studies [48-62] used a

case-control design and 13 studies [63-75] were

cross-sectional surveys The LRI outcome reported was acute

respiratory infection in seven studies [19,23,31,42,

61,63,72], bronchiolitis in ten studies [36,48-50,53,55,

56,59,64,73], bronchitis in ten studies [20,24,27,28,33,57,

66,70,71,76], pneumonia in three [54,60,75], and in 30

stu-dies the type of lower respiratory infection was not

speci-fied [17,18,21,22,25,26,29,30,32,34,35,37-41,43-47,51,

52,58,62,65,67-69,74] Studies measured infant exposure to

passive smoke either by self-report [17-22,24-28,

30-34,36,38-40,42,43,45,47-51,53-57,59-72,74-76],

inde-pendent observation [23], or by biochemically validated

measures of nicotine metabolites such as cotinine

[35,37,41,44,46,52,58,73] Thirty studies [17,18,24,25,29,

34,35,38,40,43,46,48-50,52,53,56-62,66-70,75,76] adjusted

for the infant’s age in the analysis and 46 studies

[17-22,24,26,28-35,37-39,43,45-50,52,56-71,73-75] adjusted

for other potential confounding variables, such as breast

feeding, maternal age, infant gender, allergy status,

socio-economic status, and maternal education

Methodological quality of studies and publication bias The methodological quality of the 60 studies included in the meta-analysis, as judged by the Newcastle-Ottawa scale score, is presented in Additional file 1 The overall median score was six (range three to nine) Using the

a priori chosen cut of seven to indicate high methodolo-gical quality, we judged 20 of the studies to be of high quality; and the remaining 40 to be of lower quality pri-marily due to a combination of a lack of biochemical validation of passive smoke exposure, lack of representa-tiveness of the study sample, and/or lack of adjusted analyses There was no evidence of publication bias identified from funnel plots The funnel plot for any household exposure and the risk of LRI is presented in Figure 2

Effects of any household member smoking Exposure to smoking by any household member was associated with a statistically significant increase in the odds of LRI for infants under the age of two years,

by 1.54 (95% CI 1.40 to 1.69; 37 studies; Figure 3) Moderate levels of heterogeneity (I2

) were seen in the

Figure 2 Funnel plot for household passive smoke exposure against lower respiratory infection Plot shows the standard error of the odds ratio versus odds ratio for each study (random effects model) Vertical dotted lines indicate pooled effect estimate; and dots, individual studies.

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Study or Subgroup 8.1.1 Acute respiratory infection

Blizzard 2003 Bonu 2004 Etiler 2002 Kristensen 2006

Subtotal (95% CI)

Heterogeneity: Tau² = 0.02; Chi² = 5.98, df = 3 (P = 0.11); I² = 50%

Test for overall effect: Z = 2.74 (P = 0.006)

8.1.2 Bronchiolitis

Al-Shehri 2005 Anderson 1988 Breese Hall 1984 Chatzimichael 2007 Hayes 1989 McConnochie 1986 Reese 1992

Test for overall effect: Z = 7.32 (P < 0.00001)

8.1.3 Bronchitis

Chen 1988 Fergusson 1985 Gergen 1998 Hakansson 1992 Jin 1993 Leeder 1976 Lister 1998

8.1.4 Unspecified lower respiratory infection

Baker 2006 Broor 2001 Chen 1994 Duijts 2008 Ekwo 1983 Ferris 1985 Forastiere 1992 Gardner 1984 Koch 2003 Margolis 1997 Nuesslein 1999 Ogston 1985 Ogston 1987 Pedreira 1985 Rylander 1995 Taylor 1987

8.1.5 Pneumonia

Hassan 2001 Suzuki 2009 Victora 1994

Total (95% CI)

Heterogeneity: Tau² = 0.04; Chi² = 94.60, df = 36 (P < 0.00001); I² = 62%

Test for overall effect: Z = 8.85 (P < 0.00001) Test for subgroup differences: Chi² = 29.50, df = 4 (P < 0.00001), I² = 86.4%

IV, Random, 95% CI

1.59 [1.19, 2.12]

1.15 [0.99, 1.33]

1.07 [0.80, 1.43]

1.45 [1.08, 1.94]

1.27 [1.07, 1.51]

2.51 [1.69, 3.73]

1.99 [1.00, 3.96]

4.78 [1.75, 13.01]

2.20 [1.34, 3.60]

3.86 [0.81, 18.41]

3.21 [1.42, 7.25]

2.15 [0.76, 6.10]

2.51 [1.96, 3.21]

1.25 [1.03, 1.52]

1.56 [1.15, 2.12]

1.97 [1.43, 2.71]

3.25 [1.27, 8.35]

1.78 [1.18, 2.68]

1.96 [1.37, 2.80]

0.91 [0.56, 1.47]

1.58 [1.27, 1.98]

1.29 [1.01, 1.65]

0.18 [0.02, 1.30]

1.49 [1.06, 2.10]

0.82 [0.48, 1.41]

2.09 [1.12, 3.89]

1.85 [1.56, 2.20]

1.32 [1.06, 1.65]

1.25 [0.81, 1.93]

2.13 [1.31, 3.47]

1.40 [0.93, 2.10]

1.08 [0.17, 6.80]

1.94 [0.94, 3.99]

1.68 [1.34, 2.11]

1.27 [0.97, 1.66]

2.17 [1.31, 3.59]

1.46 [1.19, 1.79]

1.49 [1.33, 1.68]

2.16 [1.42, 3.28]

1.55 [1.25, 1.92]

0.94 [0.72, 1.22]

1.43 [0.93, 2.21]

1.54 [1.40, 1.69]

0.1 0.2 0.5 1 2 5 10 Smoke decreases risk Smoke increases risk

Figure 3 Relationship between passive smoke exposure by any household member and the risk of lower respiratory infection (LRI) in infancy using a meta-analysis of comparative epidemiologic studies (Data are presented as odds ratios sub-grouped by the definition

of LRI outcome) Squares denote the odds ratio (OR) for a single study with horizontal lines denoting 95% confidence intervals The centre of the diamond denotes the pooled OR and the corners the 95% confidence intervals An OR > 1 indicates a higher risk of the outcome in those exposed to passive smoke.

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analysis (I2

= 62%) Sub-analysis based on the

defini-tion of outcome showed that the increased risk of

dis-ease was predominantly due to a strong association

between household passive smoke exposure and

bronchiolitis (OR 2.51, 95% CI 1.96 to 3.21; 7 studies;

Figure 3) Broadly similar, but lower increases in risk

were estimated for all the other categories of LRI

(ARI: OR 1.27, 95% CI 1.07 to 1.51; 4 studies;

bron-chitis: OR 1.58, 95% CI 1.27 to 1.98; 7 studies; ULRI:

OR 1.49, 95% CI, 1.33 to 1.68; 16 studies; pneumonia:

OR 1.43, 95% CI 0.93 to 2.21; 3 studies) All pooled

odds ratios were significant except for pneumonia

which was imprecisely estimated Sub-group analysis

based on study design showed similar pooled

esti-mates of increased disease risk (cohort studies: OR

1.47, 95% CI 1.33 to 1.62; 17 studies; cross-sectional

studies: OR 1.49, 95% CI 1.28 to 1.74; 11 studies;

case-control studies: OR 2.01, 95% CI 1.31 to 3.10; 9

studies) Similar pooled estimates were also seen for

sub-group analyses stratified by ascertainment of

smoking status, date of publication and

methodologi-cal quality

Effects of smoking by both parents

A pooled estimate of the 14 studies which defined

expo-sure as both parents smoking demonstrated a

statisti-cally significant increase in the odds of LRI, by 1.62

(95% CI 1.38 to 1.89; Figure 4) Moderate levels of

het-erogeneity were seen between the studies (I2

= 65%)

Sub-group analysis based on the definition of outcome

showed that the increased risk was again attributable in

particular to a strong effect on the estimated risk of

bronchiolitis (OR 3.12, 95% CI 1.76 to 5.54; 2 studies;

Figure 4), and also bronchitis (OR 2.26, 95% CI 1.50 to

3.42; 2 studies; Figure 4) Pooled estimates for the other

categories of LRI all identified statistically significant

increases in risk (ARI: OR 1.29, 95% CI 1.11 to 1.51;

2 studies; ULRI: OR 1.57, 95% CI 1.37 to 1.80; 7

stu-dies), again with the exception of pneumonia (p = 0.71,

1 study) In a sub-group analysis based on the method

of ascertainment of passive smoke exposure, studies that

used biochemically validated measures were significantly

more likely (test for sub-group differences, p = 0.006) to

show an increased risk of LRI (OR 2.69, 95% CI 1.75 to

4.13; 2 studies) than to studies that used self-reported

data (OR 1.53, 95% CI 1.31 to 1.78; 12 studies) Similar

pooled results were seen when the studies were

cate-gorised by methodological quality, date of publication,

and by study design

Effects of paternal smoking

Meta-analysis of the 21 studies of paternal smoking

demonstrated a statistically significant increase in the

odds of LRI by 1.22 (95% CI 1.10 to 1.35) Pooled

estimates for each of the outcome categories showed similar effect estimates by disease definition; however, these effects were significant only for bronchitis (OR 1.29, 95% CI 1.03 to 1.62; 3 studies) and unspecified lower respiratory infection (OR 1.26, 95% CI 1.08 to 1.45; 13 studies) In a sub-group analysis based on method of ascertainment of passive smoke exposure, similar pooled estimates for both self-reported (OR 1.24, 95% CI 1.13 to 1.36; 17 studies) and biologically validated (OR 1.26, 95% CI 0.62 to 2.54; 4 studies) measures were seen, although the latter was not sta-tistically significant (p = 0.52) Similar pooled esti-mates were also shown for the sub-group analysis of methodological quality, study design and date of publication

Effects of pre-natal maternal smoking Pooled estimates from the ten studies of pre-natal maternal smoking showed a statistically significant increase in the odds of LRI by 1.24 (95% CI 1.11 to 1.38) High levels of heterogeneity were seen between the studies (I2

= 77%) This effect was stronger in the single study of bronchitis as outcome (OR 2.44, 95%

CI 1.74 to 3.40); effects on ARI (OR 1.54, 95% CI 1.12

to 2.11; 1 study) and ULRI (OR 1.12, 95% CI 1.04 to 1.21; 8 studies) were weaker In a sub-group analysis based on method of ascertainment of passive smoke exposure, studies that used self-reported data showed

a statistically significant increase in disease risk (OR 1.25, 95% CI 1.11 to 1.40; 8 studies), in contrast to studies that used biochemical validation (OR 1.07, 95% CI 0.61 to 1.90; 2 studies) Similar pooled estimates were shown for the sub-group analysis of methodological quality, and study design All of the studies included in this exposure group were pub-lished after 1997

Effects of maternal smoking after birth Maternal smoking after birth was associated with a sta-tistically significant increase in odds of LRI, by 1.58 (95% CI 1.45 to 1.73; 31 studies; Figure 5) Sub-group analysis demonstrated a strong association between post-natal maternal smoking and bronchiolitis (OR 2.51, 95% CI 1.58 to 3.97; 5 studies; Figure 5) Pooled estimates for the other categories of LRI were similar and significant (ARI: OR 1.59, 95% CI 1.23 to 2.05; 3 studies; bronchitis: OR 1.49, 95% CI 1.25 to 1.78; 5 studies; ULRI: OR 1.64, 95% CI 1.46 to 1.84; 17 dies), with the exception of pneumonia (p = 0.87, 2 stu-dies) Sub-group analysis based on study design showed similar pooled estimates of increased disease risk (cohort studies: OR 1.62, 95% CI 1.46 to 1.79; 16 studies; cross-sectional studies: OR 1.46, 95% CI 1.18

to 1.80; 6 studies; case-control studies: OR 1.73, 95%

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CI 1.23 to 2.44; 9 studies) In a sub-group analysis

based on method of ascertainment of passive smoke

exposure similar pooled estimates for both

self-reported (OR 1.60, 95% CI 1.47 to 1.74; 26 studies)

and biologically validated (OR 1.58, 95% CI 0.95 to

2.63; 5 studies) measures were seen, although the latter was not statistically significant Similar pooled esti-mates were also shown for the sub-group analysis based on methodological quality and date of publication

Study or Subgroup

2.1.1 Unspecified lower respiratory infection

Ekwo 1983

Ferris 1985

Forastiere 1992

Ogston 1985

Ogston 1987

Rylander 1995

Taylor 1987

Fergusson 1985

Leeder 1976

Gurkan 2000

Reese 1992

2.1.4 Pneumonia

Victora 1994

Heterogeneity: Not applicable

2.1.5 Acute respiratory infection

Maziak 1999

Rahman 1997

Total (95% CI)

Test for subgroup differences: Chi² = 26.49, df = 4 (P < 0.0001), I² = 84.9%

1.59 [0.73, 3.44]

1.36 [1.11, 1.66]

1.34 [1.03, 1.75]

2.76 [1.28, 5.96]

1.74 [1.33, 2.27]

2.23 [1.23, 4.05]

1.69 [1.34, 2.14]

1.57 [1.37, 1.80]

1.83 [1.22, 2.74]

2.79 [1.87, 4.15]

2.26 [1.50, 3.42]

2.31 [0.53, 10.10]

3.29 [1.76, 6.14]

3.12 [1.76, 5.54]

0.94 [0.69, 1.29]

0.94 [0.69, 1.29]

1.24 [1.03, 1.50]

1.41 [1.07, 1.85]

1.29 [1.11, 1.51]

1.62 [1.38, 1.89]

Smoke decreases risk Smoke increases risk Figure 4 Relationship between passive smoke exposure by both parents and the risk of lower respiratory infection (LRI) in infancy using a meta-analysis of comparative epidemiologic studies (Data are presented as odds ratios sub-grouped by the definition of LRI outcome) Squares denote the odds ratio (OR) for a single study with horizontal lines denoting 95% confidence intervals The centre of the diamond denotes the pooled OR and the corners the 95% confidence intervals An OR > 1 indicates a higher risk of the outcome in those exposed to passive smoke.

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Study or Subgroup 9.1.1 Unspecified lower respiratory infection

Arshad 1993 Broor 2001 Ekwo 1983 Ferris 1985 Forastiere 1992 Koch 2003 Marbury 1996 Ogston 1985 Ogston 1987 Puig 2008 Rantakallio 1978 Rylander 1995 Stern 1989 Tager 1993 Taylor 1987 Woodward 1990 Wright 1991

Braback 2003 Fergusson 1985 Harlap 1974 Lister 1998 Mok 1982

Gurkan 2000 McConnochie 1986 Noakes 2007 Reese 1992 Sims 1978

9.1.4 Pneumonia

Victora 1994

Heterogeneity: Not applicable Test for overall effect: Z = 0.16 (P = 0.87)

9.1.5 Acute respiratory infection

Blizzard 2003 Kristensen 2006 Weber 1999

Total (95% CI)

Heterogeneity: Tau² = 0.03; Chi² = 70.12, df = 30 (P < 0.0001); I² = 57%

Test for overall effect: Z = 9.95 (P < 0.00001) Test for subgroup differences: Chi² = 17.00, df = 4 (P = 0.002), I² = 76.5%

2.24 [1.51, 3.32]

3.11 [0.05, 183.77]

1.32 [0.75, 2.32]

1.69 [1.46, 1.96]

1.21 [0.99, 1.48]

1.66 [1.12, 2.47]

1.50 [1.25, 1.80]

2.68 [1.41, 5.10]

1.52 [1.22, 1.89]

0.73 [0.49, 1.08]

1.89 [1.55, 2.30]

2.04 [1.27, 3.28]

1.85 [1.54, 2.23]

3.16 [1.24, 8.04]

1.63 [1.35, 1.97]

2.43 [1.64, 3.61]

1.52 [1.07, 2.15]

1.64 [1.46, 1.84]

1.70 [1.52, 1.90]

1.83 [1.34, 2.49]

1.43 [1.17, 1.75]

0.91 [0.56, 1.47]

1.26 [0.83, 1.92]

1.49 [1.25, 1.78]

3.60 [0.71, 18.24]

2.33 [1.19, 4.57]

2.43 [0.64, 9.26]

2.65 [0.99, 7.12]

2.51 [1.58, 3.97]

1.02 [0.80, 1.30]

1.02 [0.80, 1.30]

1.74 [1.27, 2.38]

1.38 [0.87, 2.18]

0.97 [0.21, 4.38]

1.59 [1.23, 2.05]

1.58 [1.45, 1.73]

Smoke decreases risk Smoke increases risk Figure 5 Relationship between passive smoke exposure by maternal smoking after birth and the risk of lower respiratory infection (LRI) in infancy using a meta-analysis of comparative epidemiologic studies (Data are presented as odds ratios sub-grouped by the definition of LRI outcome) Squares denote the odds ratio (OR) for a single study with horizontal lines denoting 95% confidence intervals The centre of the diamond denotes the pooled OR and the corners the 95% confidence intervals An OR > 1 indicates a higher risk of the outcome

in those exposed to passive smoke.

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Exposure-response relationships

An assessment of the relation between amount of

expo-sure and disease risk was included in 26 of the 60

papers studied, quantifying exposure in terms of the

numbers of cigarettes per day smoked by the source of

exposure, the mean daily cigarette exposure of the

infant, or by the number of smokers within the

house-hold A positive, but not necessarily significant

associa-tion was identified in 25 studies and an inverse

relationship in one

Discussion

Passive smoking was recognised as a cause of lower

respiratory infection in children in the US Surgeon

General report of 2006 [1] and also in the UK

Govern-ment SCOTH report [4] Both reports drew on a series

of systematic reviews and meta-analyses which for LRI

originally included studies published up to 1997 [3],

but was updated for the Surgeon General and SCOTH

reports [1,4] by the inclusion of papers published to

the end of 2001 The number of relevant studies has

increased substantially since the original systematic

review was published however, and the updated

sys-tematic review and meta-analysis described in the

pre-sent study combines data from 31 of the studies used

in the original review [3] with a further 29 studies

published since 1997 This study demonstrates

signifi-cant increases in the risk of LRI for smoking by the

mother, father, both parents, and by any household

member These effects are typically strongest for

bronchiolitis, and particularly in relation to maternal

smoking Pre-natal maternal smoking, which would be

expected to be confounded with post-natal smoking

because the majority of mothers who smoke through

pregnancy continue to smoke post-delivery, also had

an effect on LRI risk but this was weaker than most

natal effect estimates This indicates that

post-natal tobacco smoke exposure, rather than exposure to

blood-borne tobacco toxins in utero, is more likely to

be the underlying cause of lower respiratory infections

such as bronchiolitis in infancy

The larger number of studies now available allowed us

to explore effects on individual diagnoses included in

the LRI category, and we found that the effect of passive

smoking was typically strongest for bronchiolitis, and in

some cases bronchitis The magnitudes of the effects we

detected were broadly consistent with the original

review [3] though slightly smaller for post-natal

mater-nal smoking (1.58 versus 1.72) and patermater-nal smoking

(1.22 versus 1.29) This may indicate that publication

bias could have increased the magnitude of these earlier

estimates; however, our funnel plot analysis for passive

smoke exposure by any household member indicated

that publication bias is unlikely to have had a marked effect on the results of the present study

Our findings are likely to be representative estimates

of the true effects of passive smoking on the risk of LRI in infancy since they are based on results of a comprehensive search, including data identified through hand searching of reference lists and previous reviews However, there are limitations to this review

We elected to keep methods consistent with the origi-nal strategy [3] and only included studies written in English in the meta-analyses Additionally, we were inevitably limited in the range of confounding factors that could be adjusted for in our analyses Although the high quality studies generally adjusted for maternal age and socioeconomic status; other potential confoun-ders, such as smoking by other individuals in the household, were not consistently adjusted for in the analyses of the individual effects of paternal and maternal smoking

Conclusions This study thus confirms that exposure to all types of passive smoke, in particular maternal smoking, causes a statistically significant increase in the risk of infants developing lower respiratory infections in the first two years of life, and provides further precision in the esti-mates of the magnitudes of those effects in relation to differences in the source and extent of passive smoking

in the home Importantly, the study also identifies clini-cally-diagnosed bronchiolitis as a particular consequence

of exposure, and one which can cause significant mor-bidity and in some cases mortality Lower respiratory infections are common in infants, resulting, for example,

in over 33,000 hospital admissions in infants aged under two years in England alone, where about 10% are esti-mated to be due to passive smoke exposure [5] These additional hospital admissions are a significant public health burden all of which are avoidable It is thus clear that there is a need for renewed efforts to prevent the exposure of infants to passive smoke, both during and after pregnancy

Additional material

Additional file 1: Summary of studies included in the meta-analysis The data provided represent a summary of each of the studies included

in the updated meta-analysis.

Acknowledgements This work was supported by project grant C1512/A11160 from Cancer Research UK, and by core funding to the UK Centre for Tobacco Control Studies http://www.ukctcs.org from the British Heart Foundation, Cancer Research UK, Economic and Social Research Council, Medical Research

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Council, and the Department of Health, under the auspices of the UK

Clinical Research Collaboration.

Author details

1

UK Centre for Tobacco Control Studies, Division of Epidemiology and Public

Health, University of Nottingham, Clinical Sciences Building, Nottingham City

Hospital, Nottingham, NG5 1PB, UK.2Division of Community Health Sciences,

St George ’s University of London, Cranmer Terrace, London, SW17 ORE, UK.

Authors ’ contributions

LLJ reviewed the full text articles, extracted data and wrote the initial draft

of the manuscript AH conducted the literature search, reviewed titles,

abstracts and full text articles and contributed to the extraction of data TM

reviewed titles and abstracts and provided critical revision of the manuscript.

DGC and JB contributed to the critical revision of the manuscript JLB

reviewed titles, abstracts and full text articles, extracted data and conducted

the statistical analysis and provided critical revision of the manuscript All

authors read and approved the final manuscript.

Competing interests

The authors declare that they have no competing interests.

Received: 13 October 2010 Accepted: 10 January 2011

Published: 10 January 2011

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